The intense vasoconstriction that occurs in the renal vascular bed as a result of increased activity of the sympathetic nervous system can be caused by two mechanisms in the dog: 1) Activation of the renal sympathetic efferent nerves and 2) Adrenal catecholamines reaching the kidney via an adreno-renal vascular network. Both of these sympathetic mechanisms facilitate renal retention of sodium. Experimentally-induced cardiac arrhythmias have been used to elicit these sympathetic mechanisms in the pentobarbital anesthetized dog because with the onset of a tachyarrhythmia there is an abrupt decrease in mean arterial pressure and cardiac output which results in an immediate compensatory increase in sympathetic tone (activation of the renal sympathetic nerves). Upon cessation of an arrhythmia there is rapid return to control levels of flow in all vascular beds except the renal. The principal investigator found that this post-arrhythmic renal vasoconstriction is due to catecholamines which reach the kidney from the adrenal medulla without entering the systemic circulation via an adreno-renal vascular network. The next objective of this proposal is to determine the receptor which activates adrenal catecholamines to flow through the adreno-renal vascular network to produce post-arrhythmic renal vasoconstriction and to learn whether other cardiovascular responses not related to cardiac arrhythmias activate this receptor. Other objectives are to investigate the importance of these sympathetic mechanisms in the renal retention of sodium during the development of hypertension in the spontaneously hypertensive rat and congestive heart failure in the dog (animal models in which there is chronically increased activity of the sympathetic nervous system).